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The cardio-respiratory effects of intra-abdominal hypertension: Considerations for critical care nursing practice

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Abstract

Intra-abdominal hypertension can be classified as either primary or secondary. Primary intra-abdominal hypertension is often associated through trauma or diseases of the abdominopelvic region such as pancreatitis or abdominal surgery, while secondary intra-abdominal hypertension is the result of extra-abdominal causes such as sepsis or burns. The critically ill patient offers some challenges in monitoring in particular secondary intra-abdominal hypertension because of the effects of fluid resuscitation, the use of inotropes and positive pressure ventilation. Recent work suggests that intensive care unit nurses are often unaware of the secondary effects of intra-abdominal pressure and therefore this is not monitored effectively. Therefore being aware of the cardio-respiratory effects may alert theintensive care nurse nurse to the development of intra-abdominal hypertension. The aim of this paper is to discuss the pathophysiology associated with the cardio-respiratory effects seen with intra-abdominal hypertension in the critically ill. In particular it will discuss how intra-abdominal hypertension can inadvertently be overlooked because of the low flow states that it produces which could be misconstrued as something else. It will also discuss how intra-abdominal hypertension impedes ventilation and respiratory mechanics which can often result in a non-cardiogenic pulmonary oedema. To close, the paper will offer some implications for critical care nursing practice.

Introduction

Sustained intra-abdominal hypertension (IAH) can lead to abdominal compartment syndrome, a condition which if left untreated can lead to renal and cardiorespiratory complications and iscahemic bowel. Defined as a steady-state pressure within the abdominal cavity, intra-abdominal pressure (IAP) is governed by the elasticity of the abdominal wall and by the characteristics of the abdominal contents (Malbrain et al., 2006). Whereas IAH is defined as: “a sustained or repeated pathophysiological elevation in IAP  12 mmHg” (Malbrain et al., 2006; p1724). IAP can be classified according to the extent of intra-abdominal involvement and the degree of organ dysfunction ranging from mild IAH (Grade I: IAP 12–15 mmHg) to severe (Grade IV: IAP >25 mmHg) (Papavramidis et al., 2011). However, Kirkpatrick et al. (2013) suggests that this pressure can be as low as 12 mmHg. This differs in the critically ill were IAH has been found to be 5–7 mmHg (Fig. 1) (Malbrain et al., 2006).

Normal intra-abdominal pressure (IAP) is generally considered to be within the range of 0–7 mmHg (mean 5 mmHg ± 2.9; 0–9 cmH2O) (Sanchez et al., 2001). What determines IAP has generated considerable debate, the most reasonable explanation is following Pascal’s law of fluid mechanics in relation to the transmission of fluid-pressure. Pascal states that any change in pressure in an enclosed fluid is transmitted equally and undiminished to every part of the fluid (Walker, 2016). Therefore, with the abdomen considered an enclosed fluid filled container any change in pressure will be equally distributed through-out the abdomen (Malbrain and De Waele, 2013). However, earlier work reported that abdominal pressures fluctuate as a result of diaphragmatic flattening and gravitational forces suggesting that intra-abdominal pressure may be more dependent on the displacement of abdominal contents (Decramer et al., 1984) (Fig. 2). In measuring intra-abdominal pressure in the dog model Loring et al. (1994) found normal IAP is reliant on three factors: gravity, uniform compression and shear deformation.

Normally the abdominal cavity contains fluid that moves freely around and supports the viscera (Fig. 3a). But as the abdominal contents shift with patient positioning to the upright position, the weight of the contents significantly increases intra-abdominal pressure in the lower abdominal quadrants (Fig. 3b). Loring et al. (1994) demonstrated a positive correlation between the distance and gravitational pressure gradients measured at the xiphoid process and the bladder. The pressure gradients showed an average pressure increase of 0.90 cmH2O/centimetre (cm) (0.66 mmHg/cm) away from the xiphoid process in the up-right position (0.90 ± 0.09 cmH2O/cm; R  0.966). The lateral, prone and supine positions did show some gravitational changes but not to the same extent.

Uniform compression which can be described as diaphragmatic and rib cage flattening as well as abdominal contraction for which the abdominal contents are compressed (Fig. 3c). Unlike pure gravitational pressures, uniform compression is spatially homogenous throughout the abdomen with fluctuations dependent on diaphragmatic and abdominal muscle contraction. An example of this is the initiation of the vomiting reflex where the abdominal viscera are compressed between the descending flattened diaphragm and the contracting abdominal muscles. However uniform compression can be superimposed on gravitational pressures and patient positioning. For example patient positioning can influence IAP from between 6 mmHg (lateral position) to 16 mmHg (semi-Fowlers position). In addition, a high body mass index (BMI) will result in abdominal compression with an increase in IAP by 8–13 mmHg respectively Sanchez et al. (2001). One possible explanation is the weight of the adipose tissue having a direct compression effect on intra-abdominal contents (Fig. 2) (Frezza et al., 2007).

Shear deformation differs again from gravitational forces and uniform compression in as much that this pressure is often associated with deformation of the tissue itself as would be seen with intestinal oedema for example. The effect of intestinal oedema is not uniform throughout the abdomen and as such there may well be variations in abdominal pressure gradients as oedematous tissue displaces or compresses less oedematous tissue surrounding it (Loring et al., 1994). This is different from conditions such as abdominal ascites where the pressures generated are as a result of the excess fluid in the abdomen acting more homogenously throughout (uniform compression) and as such the IAP can remain constant.

Blood supply to the abdominal organs is extremely complex. Approximately 25% of the systemic blood volume resides here and it receives almost 30% of the cardiac output (1500 mls/min), with 30% of this volume going directly to the liver (Gallacher et al., 1999). The three main arterial systems that supply blood to the gut are the coeliac (CA), the superior mesenteric (SMA) and the inferior mesenteric arteries (IMA). The CA supplies blood to the stomach, spleen and the pancreas, the SMA to the small intestine and IMA to the large intestine. Venous outflow from these areas are directed towards the portal vein, the liver, the hepatic vein and then onto the inferior vena cava (Craft et al., 2015).

The pathophysiology of IAH is the result of either a physiologic insult such as complex abdominal surgery to critical illness for example pancreatitis or sepsis (Cheatham, 2009). This results in a complex interplay of inflammatory mediators which increase capillary permeability leading to tissue engorgement, oedema and the formation of abdominal ascites (Spencer et al., 2008). There are a number of identified risk factors that often result in IAH (Table 1) usually those associated with increased or decreased abdominal volume/compliance and in some cases both (Malbrain et al., 2006).

IAH has a widespread systemic effect as well as those confined to the abdominal compartment (De Waele et al., 2011). While there has been much emphasis on the IAH in terms of renal dysfunction, the condition has also been reported to affect liver function, as well as cardiorespiratory dynamics and intra-cranial pressure (Spencer et al., 2008, Malbrain and De Laet, 2009, Lee, 2012).

Cardiac dysfunction in the presence of IAH is generally related to two important factors:impaired venous return and direct cardiac compression; this is because up to nearly 80% of IAP is transmitted to the chest (Table 2). The inferior vena cava (IVC) enters the chest through the diaphragm at T8 and therefore the upright elevation of the diaphragm as a result of IAH constricts the IVC thereby by reducing blood flow back to the right atrium. The low pressure pulmonary vascular system is compressed leading to pulmonary hypertension with elevations in pulmonary artery wedge pressure and pulmonary vascular resistance which might be misinterpreted as hypervolaemia. Right ventricular afterload ensues because of the increase in pulmonary vascular resistance with a concomitant rise in right atrial pressure. The increase in right atrial pressure is then transmitted back through the subclavian system to the internal and external jugular veins increasing intra-cranial pressure. Reduced left ventricular compliance and contractility occurs because of displacement or bulging of the inter-ventricular septum from right to left further reducing left ventricular diastolic filling. The Frank-Starling curve as it relates to left ventricular contractility is displaced downwards as a reduced left ventricular pre-load diminishes cardiac output (Malbrain and De Waele, 2013). However, mean arterial pressure is often maintained for three reasons. First increased intra-thoracic pressure compresses the aorta resulting in an increased afterload (Malbrain and De Waele, 2013). Second the reduction in renal blood flow initiates the renin-angiotensin aldosterone pathway as a means of increasing systemic vascular resistance and fluid retention, to increase afterload and increase pre-load in response to low circulating blood volume (Scheppach, 2009). Finally, sympathetic nervous system stimulation, direct compression of vascular beds and venous congestion also contribute to the increasing afterload, although the latter is not through any compensatory mechanism rather as a result of reduced blood flow retuning to the right atrium and the resultant back pressure inferiorly from the diaphragm (Mohmand and Goldfarb, 2011).

In the spontaneously breathing patient it can be seen from the normal pressure-volume curve that airway resistance and alveolar opening require lower opening pressures to promote alveolar recruitment (Fig. 4a). However, with decreased chest wall compliance caused by the elevated diaphragm this shifts the lower inflection point on the pressure-volume curve to the right, in essence flattening the initial inspiratory part of the curve with a concomitant rise in airway resistance (Fig. 4b). This means that as elastic recoil of the chest wall increases and compliance decreases it increases alveolar opening pressure (Fig. 4b). The increase in alveolar opening pressure increases the work of breathing, but in doing so causes a reduction in gas flow to dependent areas of the lung such as the lower lobes (Pelosi et al., 2007). It is the flow limitation that eventually gives rise to atelectasis in these areas. As the work of breathing increases as does the respiratory rate, less proportion of the inspiratory gas flow goes to these areas and eventually they become less complaint and collapse. In addition the trans-pulmonary pressure decreases; this is the pressure difference between pleural and alveolar pressures and is affected by the lungs elastic recoil, therefore the lower the trans-pulmonary pressure the harder it is to breathe. This results in higher opening pressures to aid in alveolar recruitment and alveolar opening (Fig. 4b) (West, 2005).

While chest wall mechanics in the presence of IAH has a direct effect on respiratory compliance it has been linked to secondary acute lung injury and adult respiratory distress syndrome (Pelosi et al., 2007). As IAH causes increased chest wall elasticity it also promotes a reduction in the functional residual capacity (Harris, 2005). The resultant increase in peak airway pressure and plateau pressure causes barotrauma to alveolar structures thereby promoting a neutrophil activated inflammatory response. This promotes increased capillary permeability and protein rich fluid leakage into the pulmonary interstitial space, the result is the development of non-cardiogenic pulmonary oedema. The increased presence of pulmonary interstitial fluid often occurs because of poor lymphatic drainage. This happens not only because of the rise in lymphatic fluid draining from the interstitial space where the lymphatic system eventually becomes overwhelmed, but also as a product of the increased thoracic pressure caused by IAH and the compression of the lymph channels in particular those feeding into the thoracic duct. The thoracic duct itself originates in the abdomen where lymph empties via this duct from the lower and upper left side of the body into the left subclavian vein (Guyton and Hall, 2015); therefore the effects of oedema are not isolated to the pulmonary lymphatics. Thoracic duct compression along with the inflammatory response mentioned above also effects the splanchnic circulation further worsening the IAH as abdominal organs become engorged and oedematous promoting the formation of ascites (Malbrain et al., 2007).

Intra-abdominal hypertension in the critically ill falls within two specific categories either primary or secondary causes. Primary IAH is associated with conditions that originated in the abdominopelvic region, while secondary IAH is the result of extra-abdominal causes such as sepsis (Malbrain et al., 2006). Primary IAH is easily recognisable because of the presenting problem and therefore measures to identify and monitor IAH are relatively simple (Reintam et al., 2008). However, what is more challenging are those patients that develop secondary IAH for which routine monitoring is often overlooked (Jakob et al., 2010). For example, Reintam et al. (2008) found that patients who had developed secondary IAH had a higher mortality rate than those with a primary source of IAH. Yet they also found that the development of secondary IAH was more insidious, took longer to develop and lasted longer than primary IAH. Some studies suggest aggressive fluid resuscitation in the secondary group might be a contributing factor (Balogh et al., 2007) while others suggest that body mass index is a strong indicator of chronic IAH and therefore can easily transgress to acute IAH (Frezza et al., 2007). As mentioned previously obesity, just by the sheer weight of the adipose tissue compressing the abdomen, can increase IAP threefold (Pelosi et al., 2007, De Keulenaer et al., 2009). Compound this with critical illness, fluid resuscitation, inotropic support and positive pressure ventilation in conjunction with positive end expiratory pressure (PEEP); it is easy for secondary IAH to develop.

It is well recognised that treatment modalities in critical illness such as fluid resuscitation and the use of inotropes will cause variations in regional blood flow and the most susceptible area is the splanchnic region. Splanchnic hypoperfusion, fluid third-spacing, and bowel oedema creates a vicious cycle of bowel ischemia that can eventually lead to IAH. However, the use of positive pressure ventilation in particular the use ofpositive end expiatory pressure (PEEP) is an important consideration that is not often contemplated especially in the patient with IAH. The benefits of PEEP are well documented in the literature: improved oxygenation, improved alveolar recruitment, increased functional residual capacity and improved lung compliance (Acosta et al., 2007, Gattinoni et al., 2010, Sundaresan and Chase, 2012). Yet, the use of PEEP has been implicated in a worsening of IAH as a result of diaphragmatic excursion, the effect of which is an elevation of IAP (Fig. 5) in some cases by 8–39% (Ferrer and Molina, 2008). This occurs as PEEP shifts the pressure-volume curve to the right, the added pressure is then transmitted into the abdomen. What occurs is a shift in the lower inflection point and while benefiting pulmonary compliance, this point then becomes an approximation of IAP (Malbrain and De Waele, 2013). In addition some studies have demonstrated that the application of PEEP to support acute lung injury has the deleterious effect of reducing splanchnic blood flow further promoting bowel hypoperfusion (Morejon and Barbeito, 2012). Verzilii et al.’ (2010) pilot study looking at the use of PEEP and the effects on IAP found that at a PEEP of 12cmH2O IAP increased 3.5 mmHg from baseline (11.7 mmHg) which in effect created mild IAH (Grade 1).

Spencer et al. (2008) have clearly indicated that the critical care nurse is well situated to monitor and detect changes in the patient hemodynamic and respiratory profiles and as such be aware of the changes in these profiles could be attributed to IAH. In a recent study Hunt et al. (2016) found that critical care nurses had poor knowledge of IAH and abdominal compartment syndrome, in particular the ability to detect those patients who were at risk of developing IAH such as the obese. It is interesting to note that nurses in this study were able to initiate IAP monitoring in the primary IAH patients groups, however there was a lack of deeper knowledge and understanding as to what the IAP reading meant or implied. This is concerning considering the high mortality rate associated with secondary IAH. The authors did go onto suggest that more than 73% of the cohort identified education as key to improving IAP monitoring and 65% identified the need for more detailed protocols and policies around IAP monitoring. While monitoring is important in determining the support needed to reduce the incidence of IAH in the critically ill, there is a danger that this may simply become task focused. Therefore the considerations for critical care nursing practice are not only to suggest that monitoring is a priority, but perhaps the focus needs to identify those patients at risk and this can only come from making critical care nurses aware of some of the physiological changes that may be attributed to developing IAH. For example;

  • 1.

    Any patient having a body mass index greater than 30 should be immediately identified as a patient at risk of developing IAH;

  • 2.

    An elevated central venous pressure or a pulmonary capillary wedge pressure is not always indicative of adequate intravascular filling especially if the patient is obese because of the tendency of this patient group to potentially have chronic IAH;

  • 3.

    In the absence of cardiac output monitoring, to be aware that MAP is not necessarily a reliable measure of cardiac function in patients with IAH because of the compensatory factors associated with low flow states;

  • 4.

    The application of PEEP will raise IAP in susceptible patients such as the over-weight/obese or those with a secondary condition which might contribute to fluid shifts and therefore IAP should monitored in these patient groups – measuring the lower inflection point of the pressure-volume curve might provide a useful indicator of increasing IAP;

  • 5.

    Maintaining an abdominal perfusion pressure (APP = MAP–IAP) greater that 60 mmHg is important in ensuring an adequate perfusion to the splanchnic structures, although this does not immediately reflect an increase in urine output;

  • 6.

    Oliguria (<0.5 ml/kg/h) may well be the first sign of increasing IAP.

Although beyond the scope of this paper, accurate monitoring is the most important factor in identifying those patients at risk of or who have developed IAH so that interventions can be initiated to reduce the impact of IAH especially in terms of patient outcome.

Section snippets

Conclusion

Clearly IAH has a high mortality especially if the IAH is associated with secondary factors such as sepsis or obesity. The critical care nurse is well situated to identify the early stages of increasing IAP in the critically ill, yet research has identified that this is not always the case (Hunt et al., 2016). The cardio-respiratory effects of IAP can be easily misinterpreted as hypervolaemia. Some have called for further education in not only prompting nurses to be aware of IAH but also in its

Authors’ contribution

All authors have contributed equally to the initial development and production of the manuscript.

Conflicts of interest

There are no conflicts of interest.

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